This invention relates generally to techniques for providing treatment therapy to neural tissue to relieve visceral pain, and more particularly, but not by way of limitation, to spinal cord stimulation for the treatment of visceral pain of gastrointestinal origin, functional bowel disorders and irritable bowel syndrome.
Functional bowel disorders, including irritable bowel syndrome, are common abnormalities of the gastrointestinal tract that are associated with severe and chronic abdominal pain. It has been estimated that a minimum of 10-20% of the United States population experience several of the symptoms of functional bowel disorders. Moreover, greater than 30% of patients that recover from an acute infectious gastroenteritis also exhibit irritable bowel syndrome symptomatology. Symptoms of irritable bowel syndrome include abdominal cramping with pain that is concurrent with abnormal bowel habits in terms of frequency and appearance.
Treatments for functional bowel disorders generally, and irritable bowel syndrome specifically, include modification of diet, psychological therapy, stress management, exercise, antidepressant and antianxiety medications, antidiarrheals, bile acid binding agents, anticholinergics, some experimental medications, and other pharmacological and non-pharmocological treatments. These treatments have only limited success and effectiveness and some have undesirable side effects.
Electrical stimulation of the dorsal columns of the spinal cord (spinal cord stimulation; SCS) has been employed for years to treat chronic severe pain. Currently the applications for spinal cord stimulation include both chronic neuropathic and ischemic pain. The mechanism by which electrical stimulation via an electrode placed on the dorsal surface of the spinal cord provides pain relief is poorly understood but may involve both spinal and supraspinal neural circuits.
The symptoms of irritable bowel syndrome may be due, at least in part, to disturbed intestinal motility, primarily characterized by hypercontractility. Nevertheless, symptoms cannot be explained entirely by changes in motility alone and they may also arise from complex feedback and feed-forward interactions between supraspinal circuits, the spinal cord and the periphery.
Abnormal (or heightened) visceral sensory perception is a more recent mechanism that has been proposed to account for many of the symptoms of irritable bowel syndrome. The concept of abnormal pain perception in irritable bowel syndrome is supported by the observation that gastrointestinal distention in patients with irritable bowel syndrome evokes pain at lower distention pressures compared to asymptomatic control subjects. It may be that the development of gastrointestinal sensitization initiates the process of abdominal pain and concomitant abnormal gastrointestinal function seen in irritable bowel syndrome patients.
Visceral allodynia (nonpainful response perceived as painful) and hyperalgesia (heightened response to a painful stimulus) in patients with irritable bowel syndrome has been postulated to develop as a result of an acute irritating event followed by development of hypersensitivity of undamaged tissues. The increased sensitivity could occur as the result of central and/or peripheral mechanisms. A manifestation of these changes is that responses to colorectal distention are accentuated in animals with visceral hypersensitivity. For example, colonic inflammation with mustard oil has been found to increase the background activity in lumbosacral postsynaptic dorsal column neurons and potentiated the evoked responses to colorectal distention.
In response to sensitization, innocuous colorectal distentions evoke a visceromotor behavioral response, which resemble those induced by nociceptive stimuli in non-sensitized rats. This suggests that alterations in neuronal activity within the spinal cord may be involved in processing information from the colon, and that induced abnormalities in spinal neuronal processing may lead to the development of visceral hypersensitivity. Furthermore, recent animal studies have shown that nociceptive distention of the colon produces an increase in cFos expression (a gene marker indicating enhanced neuronal excitability) in the lumbosacral spinal cord suggesting enhanced neuronal excitability. Pharmacotherapy of similar symptoms encountered in man often fails, and spinal cord stimulation besides its beneficial effects on various types of pain also has proven effective in suppressing hyperexcitable somatosensory reflexes in spasticity.
Despite studies and postulates, however, chronic visceral pain of gastrointestinal origin is poorly understood and lacks an effective therapy. Thus, there is a need for improved treatment for visceral pain of gastrointestinal origin, functional bowel disorders and irritable bowel syndrome.